A 30 year old woman has been certifted "brain dead". While awaiting organ donation she ishypotensive, polyuric and hypothermic. Outline your management.
Efficient support of the potential organ donor is an integral part of IC practice. Since we know nothing of this patient's story a back to basics detailed approach to the patient should have included:
(a) Check airway patency, tube position.
(b) Ensure adequate ventilation:
• Examination, ABG, CXR (to exclude pneumothorax/lung injury, hypoxialhypercarbia) (c) Restore circulation with fluid challenge. Assess filling pressures and response to challenge.
• If diabetes insipidus is apparent (eg. urine output >300mlslhr, serum osmolality >300, urine osmolality <300 in the absence of diuretics) give lug ofDDAVP lV or SC
• If restoration of fluid status does not restore BP and organ perfusion, commence vasoconstrictor infusion (aramine or noradrenaline)
• Moderate hypothermia (35°C} may be well tolerated and require no specific therapy
• Persistent hypotension in the presence of impaired pituitary functiODt as evidenced by DI. It may be an indication for intravenous corticosteroids and T3. There usually is no time for a random cortisol level
• Maintain fluid and electrolyte homeostasis eg. replacing urine output ml for ml
This question discussess the generic principles of care for the brain-dead organ donor. This issue is explored in great depth in the answer to Question 1 from the first paper of 2012:
"Outline the Intensive Care management of a 25-year-old male who has fulfilled brain death criteria and is awaiting surgery for organ donation."
Non-clinical issues: (presumably, these have been dealt with now that the patient is "awaiting surgery for organ donation"
Summarized from the ANZIC statement on Brain Death and Organ Donation, Version 3.2
Dujardin, Karl S., et al. "Myocardial dysfunction associated with brain death: clinical, echocardiographic, and pathologic features." The Journal of heart and lung transplantation 20.3 (2001): 350-357.
Totsuka, Eishi, et al. "Influence of high donor serum sodium levels on early postoperative graft function in human liver transplantation: effect of correction of donor hypernatremia." Liver Transplantation and Surgery 5.5 (1999): 421-428.
Novitzky, D., D. K. C. Cooper, and B. Reichart. "Hemodynamic and metabolic responses to hormonal therapy in brain-dead potential organ donors." Transplantation 43.6 (1987): 852-854.
Phongsamran, Paula. "Critical care pharmacy in donor management." Progress in Transplantation 14.2 (2004): 105-113.
RANDELL, TARJA T., and KRISTER AV HöCKERSTEDT. "TRIIODOTHYRONINE TREATMENT IN BRAIN-DEAD MULTIORGAN DONORS-A CONTROLLED STUDY." Transplantation 54.4 (1992): 736-737.
Goarin, Jean-Pierre, et al. "The effects of triiodothyronine on hemodynamic status and cardiac function in potential heart donors." Anesthesia & Analgesia 83.1 (1996): 41-47.
Follette, David M., Steven M. Rudich, and Wayne D. Babcock. "Improved oxygenation and increased lung donor recovery with high-dose steroid administration after brain death." The Journal of heart and lung transplantation: the official publication of the International Society for Heart Transplantation 17.4 (1998): 423-429.
Lisman, T., et al. "Activation of hemostasis in brain dead organ donors: an observational study." Journal of Thrombosis and Haemostasis 9.10 (2011): 1959-1965.
Lim, H. B., and M. Smith. "Systemic complications after head injury: a clinical review." Anaesthesia 62.5 (2007): 474-482.
Dalle Ave, Anne L., Dale Gardiner, and David M. Shaw. "Cardio‐pulmonary resuscitation of brain‐dead organ donors: a literature review and suggestions for practice." Transplant International (2015).
Singer, Pierre, Haim Shapiro, and Jonathan Cohen. "Brain death and organ damage: the modulating effects of nutrition." Transplantation 80.10 (2005): 1363-1368.
Outline the principles involved in the care of the organ donor.
Principles include:
Early identification
Discuss with transplant coordinator
Establish family rapport early
Diagnose brain death correctly
Establish presence of condition causing brain death. Exclude confounders (sedation, paralysis, endocrine, metabolic, temperature) - use vascular imaging if necessary. Satisfy legal criteria for organ donors relevant to the jurisdiction
Non-coercive sensitive family discussion re opportunity for donation
High availability. Answer questions
Initiate tissue typing, viral screen, further organ function tests
Maintain extra-cerebral physiological stability
Ventilatory - oxygenation, normocapnia, lung protective strategies. Circulatory - monitoring, filling,
noradrenaline, vasopressin. Normothermia. Diagnose and treat diabetes insipidus
(DDAVP/vasopressin, free water). Steroid and T3 replacement
Facilitate family time at bedside
Ensure aftercare of donor family
Transplant co-ordinator. Limited anonymous information available. Further family meeting offered
Few candidates considered that the donor could be either living related, or a non-beating heart donor.
This question closely resembles Question 1 from the second paper of 2012.
Non-clinical issues: (presumably, these have been dealt with now that the patient is "awaiting surgery for organ donation"
Summarized from the ANZIC statement on Brain Death and Organ Donation, Version 3.2
Dujardin, Karl S., et al. "Myocardial dysfunction associated with brain death: clinical, echocardiographic, and pathologic features." The Journal of heart and lung transplantation 20.3 (2001): 350-357.
Totsuka, Eishi, et al. "Influence of high donor serum sodium levels on early postoperative graft function in human liver transplantation: effect of correction of donor hypernatremia." Liver Transplantation and Surgery 5.5 (1999): 421-428.
Novitzky, D., D. K. C. Cooper, and B. Reichart. "Hemodynamic and metabolic responses to hormonal therapy in brain-dead potential organ donors." Transplantation 43.6 (1987): 852-854.
Phongsamran, Paula. "Critical care pharmacy in donor management." Progress in Transplantation 14.2 (2004): 105-113.
RANDELL, TARJA T., and KRISTER AV HöCKERSTEDT. "TRIIODOTHYRONINE TREATMENT IN BRAIN-DEAD MULTIORGAN DONORS-A CONTROLLED STUDY." Transplantation 54.4 (1992): 736-737.
Goarin, Jean-Pierre, et al. "The effects of triiodothyronine on hemodynamic status and cardiac function in potential heart donors." Anesthesia & Analgesia 83.1 (1996): 41-47.
Follette, David M., Steven M. Rudich, and Wayne D. Babcock. "Improved oxygenation and increased lung donor recovery with high-dose steroid administration after brain death." The Journal of heart and lung transplantation: the official publication of the International Society for Heart Transplantation 17.4 (1998): 423-429.
Lisman, T., et al. "Activation of hemostasis in brain dead organ donors: an observational study." Journal of Thrombosis and Haemostasis 9.10 (2011): 1959-1965.
Lim, H. B., and M. Smith. "Systemic complications after head injury: a clinical review." Anaesthesia 62.5 (2007): 474-482.
Dalle Ave, Anne L., Dale Gardiner, and David M. Shaw. "Cardio‐pulmonary resuscitation of brain‐dead organ donors: a literature review and suggestions for practice." Transplant International (2015).
Singer, Pierre, Haim Shapiro, and Jonathan Cohen. "Brain death and organ damage: the modulating effects of nutrition." Transplantation 80.10 (2005): 1363-1368.
(a) Outline the situations in which clinical tests cannot be used to confirm brain death.
(b) List 2 adjunctive tests used in Australia and New Zealand for the confirmation of brain death when clinical tests are unable to be performed.
(c) List other adjunctive tests which may have a role in the diagnosis of brain death.
a) Clinical tests cannot be used to confirm brain death in a number of situations, including:
• No clear cause of coma
• Possible drug or metabolic effect on coma
• Cranial nerves cannot be adequately tested
• Cervical vertebra or cord injury present
• Cardiorespiratory instability precludes apnoea testing
• In term infants and up to 1 year of age, on the assumption that the younger brain has a greater potential for recovery, a confirmatory test is usually conducted
b) The two adjunctive tests recognized in the ANZICS guidelines are 3 or 4 vessel angiogram, and nuclear medicine study capable of imaging posterior fossa blood flow, e.g. use of nuclear study with SPECT.
c) Additional tests which may play a role (but have various limitations) are electrophysiological tests (ie. evoked potentials, EEG), transcranial doppler ultrasound, and simpler nuclear medical perfusion scans. The use of Xe-CT and specific MR sequences have been described, but seem to hold no particular advantages. In the future, CT angiogram, or CT perfusion may play a role. Neither has obvious current advantages, but if sufficiently reliable, may be more widely available. Seventeen out of twenty-six candidates passed this question.
This question closely resembles the following questions:
a) "Outline the situations in which clinical tests cannot be used to confirm brain death." - This is really a question about the preconditions for brain death testing. Thus, clinical brain death testing canot be carried out if there is no obvious cause of the coma, when the patient is desperately hypoxic and hemodynamically unstable, and when you have no intact eyes or ears to test, etc etc.
Pre-conditions for brain death testing are discussed in several other fellowship questions:
In order to simplify revision, the list of reasons for not being able to perform clinical brain death testing is replicated here:
b) " List 2 adjunctive tests used in Australia and New Zealand for the confirmation of brain death when clinical tests are unable to be performed." - This is really a question about imaging modalities to confirm brain death. Four-vessel DSA and Tc-99m HMPAO are the better two, followed by CT angiography.
Additonal tests to confirm brain death - which are not gold standard material, but which are mentioned by the ANZICS Statement on Death and Organ Donation - include the following:
As diagnostic tools for brain death these leave much to be desired (owing to poor sensitivity or specificity), but as predictors of poor neurological outcome they have merit. In this context, these diagnostic modalities are discussed at great length in Question 4 from the second paper of 2013, "Describe the clinical signs and investigations available to predict poor neurological outcome in comatose survivors of cardiac arrest".
ANZICS Death and Organ Donation Committee, THE ANZICS STATEMENT ON DEATH AND ORGAN DONATION Edition 3.2 2013
Outline the indications, advantages and disadvantages of cerebral perfusion scanning for the certification of brain death.
Indications
1. Any doubt about the primary diagnosis of the cause of coma.
2. Possible drug or metabolic cause of coma.
3. Cranial nerves can not be tested adequately e.g. periorbital oedema, eye injuries, ruptured tympanum
4. Apnoea test can not be performed e.g. cervical cord injury, cardiorespiratory instability.
5. confirmation of brain death in some countries (not ANZ)
Advantages
• Highly specific
• Does not require preconditions as for clinical testing –ie patient can be cold, hypoxic, sedated, undiagnosed, etc
• Can be done at the bedside – if portable gamma camera
• Safe – non-toxic marker (Te99m HMPAO) can be delivered via peripheral vein
• Quick – answer can be given within 30 minutes
• Provides a hard copy – clear permanent documentation of brain death
Disadvantages
• Requires specialized equipment, marker and staff (nuclear medicine specialist) usually only available in major centres
• Requires patient transport – if no portable camera
• Can show minimal flow ( e.g. from meningeal vessels), cannot easily be repeated, and not very soon after first test
This question refers specifically to the Tc-99 HMPAO SPECT scan, which (after the four-vessel DSA) is viewed by the ANZICS Statement on Death and Organ Donation as the second best way of confirming that there is no blood flow to the noggin.
The indications for imaging to confirm brain death, broadly, are as follows:
The indications for choosing a radionuclide scan, rather than a DSA, may be as follows:
Advantages of the HMPAO-SPECT:
Disadvantages of HMPAO-SPECT:
ANZICS Statement on Death and Organ Donation
Wieler, H., et al. "Tc-99m HMPAO Cerebral Scintigraphy A Reliable, Noninvaslve Method for Determination of Brain Death." Clinical nuclear medicine18.2 (1993): 104-109.
Donohoe, Kevin J., et al. "SNM practice guideline for brain death scintigraphy 2.0." Journal of nuclear medicine technology 40.3 (2012): 198-203.
Munari, Marina, et al. "Confirmatory tests in the diagnosis of brain death: comparison between SPECT and contrast angiography." Critical care medicine33.9 (2005): 2068-2073.
Joffe, Ari R., Laurance Lequier, and Dominic Cave. "Specificity of radionuclide brain blood flow testing in brain death: case report and review." Journal of intensive care medicine 25.1 (2010): 53-64.
Heran, Manraj KS, Navraj S. Heran, and Sam D. Shemie. "A review of ancillary tests in evaluating brain death." The Canadian Journal of Neurological Sciences35.4 (2008): 409-419.
Comment on the significance of the following signs in a patient on whom you are performing brain death testing:
a) a generalised tonic clonic seizure
b) slow drifting of one eye away from the ear in which cold water is injected during caloric testing
c) flexion of the arm at the elbow following imposition of a painful stimulus to the nail bed on that side
d) sitting up during apnoea testing
e) an increase in pulse from 70 bpm to 110 bpm during apnoea testing
With each of these signs, clearly indicate if they are compatible or not with the diagnosis of brain death and provide a brief explanation for your answer.
a) generalised tonic clonic seizure
the patient must have intact neural connections to have a grand mal fit - brain death can not be present
b) slow drifting of one eye away from the ear in which cold water is injected during caloric testing
any eye movement in response to caloric testing signifies the presence of some reflex arc function. Brain death cannot be diagnosed
c) flexion of the arm at the elbow following imposition of a painful stimulus to the nail bed on that side this may represents a spinal reflex. It does not influence a diagnosis of brain death
d) sitting up during apnoea testing
this represents another spinal reaction to the acidosis which occurs with hypercarbia and is termed the Lazarus sign. It usually really unsettles nursing staff and is inevitably very disturbing to relatives. However it is compatible with a diagnosis of brain death .
e) an increase in pulse from 70 bpm to 110 bpm during apnoea testing Hypercarbia (which occurs during apnoea testing) results in endogenous adrenaline release. An change in pulse rate and blood pressure is common during apnoea resting and is not incompatible with brain death
The ANZICS Statement on Death and Organ Donation is again the primary source for this answer. Specifically, I direct the reader to Page 22 of the most recent version, where sections 2.2.3 and 2.2.4 discuss observations which are compatible and incompatible with drain death.
To simplify revision, I will quote some of them here.
For a more comprehensive overview, a good (ancient) article from the Acta Neurochirurgica describes what the authors have quaintly termed "Spinal Man", a species of human bereft of higher cortical function, which is a creature reliant purely on spinal reflexes.
Additionally, a more recent article discusses the various physiological responses to apnoea testing, including all the various cardiovascular derangements which occur.
Thus:
a) - a seizure - rules out brain death
b) - a positive caloric reflex - is a brainstem reflex which is still working, and it rules out brain death
c) - arm flexion to ipsilateral painful stimulus - could be a spinal reflex, and does not rule out brain death.
d) - a Lazarus sign - does not rule out brain death
e) - a hypercapnea-associated catecholamine surge - can occur with zero cerebral input, and does not rule out brain death.
ANZICS Death and Organ Donation Committee, THE ANZICS STATEMENT ON DEATH AND ORGAN DONATION Edition 3.2 2013
McNair, N. L., and K. J. Meador. "The undulating toe flexion sign in brain death." Movement disorders 7.4 (1992): 345-347.
Jørgensen, E. O. "Spinal man after brain death." Acta neurochirurgica 28.4 (1973): 259-273.
Ropper, Allan H. "Unusual spontaneous movements in brain‐dead patients."Neurology 34.8 (1984): 1089-1089.
Heytens, Luc, et al. "Lazarus sign and extensor posturing in a brain-dead patient: case report." Journal of neurosurgery 71.3 (1989): 449-451.
Lang, C. J. G., and J. G. Heckmann. "Apnea testing for the diagnosis of brain death." Acta neurologica scandinavica 112.6 (2005): 358-369.
A 53 year old patient was admitted with a GCS of 3. The GCS has remained unchanged for 24 hours. The cause of the coma is unclear. He has had no sedation or paralysis for more than 24 hours. His temperature is 36.50C
You find the following on neurological examination
Arterial blood gases during apnoea test:
pH 7.23
PCO2 65 mm Hg (8.75kPa)
PO2 146 mm Hg (19.4 kPa)
What is your assessment of the neurological status and why?
Patient clearly has no evidence of brain stem reflexes, however, can’t be declared brain dead as there is no known cause of coma.
As in the above college answer, this patient cannot be declared brain dead.
The preconditions for brain death testing are not met; according to the ANZICS statement (linked below), "Brain death cannot be determined without evidence of sufficient intracranial pathology". In this, Australians differ to the British; in Britain it is sufficient to have a dead brainstem for a diagnosis of brain death, even with ample blood flow to the rest of the cortex.
So at this stage, one could not declare this patient brain dead without imaging which might demonstrate an absence of cerebral perfusion (or without shipping the patient to Britain).
ANZICS Death and Organ Donation Committee, THE ANZICS STATEMENT ON DEATH AND ORGAN DONATION Edition 3.2 2013
. Prior to the determination of brain death by clinical examination,
a) list the preconditions that must be met before formal testing can begin
b) What are the indications for ancillary tests for brain death (ie tests that demonstrate the absence of intracranial blood flow)?
c) What are the 2 imaging techniques currently recommended by ANZICS for determining the absence of intracranial blood flow:
Preconditions
a) A known cause of coma (check terminology in new ANZICS guidelines)
b) Minimum of 4 hour period observation
c) neuro-imaging consistent with acute brain pathology which could result in brain death;
d) temperature > 35C;
e) normotension (as a guide, systolic blood pressure > 90 mmHg, mean arterial pressure (MAP) >
60 mmHg in an adult);
f) exclusion of effects of sedative drugs: the time taken for plasma concentrations of sedative drugs to fall below levels with clinically significant effects depends on
the dose and pharmacokinetics of drugs used, and on hepatic and renal function. If there is any doubt about the persisting effects of opioids or benzodiazepines, an appropriate drug antagonist should be administered;
g) absence of severe electrolyte, metabolic or endocrine disturbances. These include marked derangements in plasma concentrations of glucose, sodium, phosphate or magnesium, liver and renal dysfunction and severe endocrine dysfunction;
h) intact neuromuscular function. If neuromuscular-blocking drugs have been administered, a peripheral nerve stimulator or other recognised method (e.g. electromyography) should always be used to confirm that neuromuscular conduction is normal;
What are the indications for ancillary tests for brain death?
° Inability to adequately examine the brain-stem reflexes. It must be possible to examine at least one ear and one eye;
° Inability to perform apnoea testing. This may be precluded by severe hypoxic respiratory failure or a high cervical spinal cord injury.
What are the 2 imaging techniques currently recommended by ANZICS for determining the absence of intracranial blood flow:
Four vessel intra-arterial catheter angiography, with digital subtraction; Tc-99 HMPAO SPECT radionuclide imaging
CT angio with certain caveats may be acceptable. Do not recommend MR angio
This question resembles several other questions in the past papers:
The pre-conditions for clinical brain death testing are:
Otherwise, this current paper asks one original question: when must one resort to imaging?
Well. The ANZICS Statement on Death and Organ Donation suggests several distinct scenarios when one cannot perform clinical brain death testing:
The following blood gases obtained at 8am and 10 am from a patient admitted to the ICU with Grade V Subarachnoid hemorrhage. Between the two sets of arterial blood gases a procedure was performed. Changes in gas tensions were not accompanied by changes in haemodynamic parameters.
|
Time |
8 AM |
10 AM |
|
FiO2 |
0.3 |
1.0 |
|
pH |
7.41 |
7.06 |
|
PCO2 |
39 mm Hg (5.2 kPa) |
108 mm Hg (14.4 kPa) |
|
PO2 |
103 mm Hg (13.7 (kPa) |
425 mm Hg (56.6 kPa) |
|
Peak airway |
24 cm water |
0 cm water |
|
Tidal |
650 ml |
0 ml |
15.1 What procedure was performed? Give reasons.
Apnoea test (as peak pressure has dropped to zero and there is no recordable TV. Not likely to be bronchoscopy as peak pressures are high during bronchoscopy
This patient is not breathing, and is demonstrating no respiratory drive in spite of a ridiculously high CO2. The 100% FiO2 suggests that an apnoea test for brain death is in progress.
Ropper, Allan H., Sean K. Kennedy, and Lisa Russell. "Apnea testing in the diagnosis of brain death: clinical and physiological observations." Journal of neurosurgery 55.6 (1981): 942-946.
Outline the preconditions that must be met in order for accurate determination of brain death by clinical examination.
• Evidence of sufficient intracranial pathology or a known cause of coma e.g.; traumatic brain injury, intracerebral haemorrhage, hypoxic-ischaemic encephaloopathy
• normothermia (temperature > 35°C);
• normotension (as a guide, systolic blood pressure > 90 mmHg, mean arterial pressure (MAP> 60 mmHg in an adult);
• exclusion of effects of sedative drugs (self-administered or otherwise) — the time taken for plasma concentrations of sedative drugs to fall below levels with clinically significant effects depends on the dose and pharmacokinetics of drugs used, and on hepatic and renal function. If there is any doubt about the persisting effects of opioids or benzodiazepines, an appropriate drug antagonist should be administered;
• absence of severe electrolyte, metabolic or endocrine disturbances— these include: marked derangements in plasma concentrations of glucose, sodium, phosphate or magnesium; liver and renal dysfunction; and severe endocrine dysfunction;
• intact neuromuscular function— if neuromuscular-blocking drugs have been administered, a peripheral nerve stimulator or other recognised method (e.g. electromyography) should always be used to confirm that neuromuscular conduction is normal;
• ability to adequately examine the brain-stem reflexes— it must be possible to examine at least one ear and one eye; and
• ability to perform apnoea testing— this may be precluded by severe hypoxic respiratory failure or a high cervical spinal cord injury.
The answer above is lifted straight from the ANZICS Statement on Death and Organ Donation (I have linked to Version 3.2, from 2013).
In brief, the preconditions are:
ANZICS Death and Organ Donation Committee, THE ANZICS STATEMENT ON DEATH AND ORGAN DONATION Edition 3.2 2013
When the preconditions for the clinical determination of brain death cannot be met, what imaging modalities are recommended to determine absence of intracranial blood flow? What findings in each test confirm brain death?
|
Test |
Positive result |
|
Four vessel angiography |
no blood flow above the carotid siphon in the anterior circulation and no blood flow above the foramen magnum in the posterior circulation |
|
Radionuclide imaging |
Tc-99m HMPAO scan demonstrating absent intracranial perfusion |
|
CT angiography |
absent enhancement bilaterally of peripheral intracranial arteries and central veins at 60 seconds. |
The answer above borrows heavily from the ANZICS Statement on Death and Organ Donation (I have linked to Version 3.2, from 2013).
In brief, the investigations and expected findings are as follows:
Four-vessel arterial digotal subtraction angiography:
Tc-99m HMPAO radionuclide (SPECT) scan
CT angiography
Outline the important management principles in treating a patient who has been admitted to your ICU intubated and ventilated immediately following successful resuscitation from an out of hospital cardiac arrest.
Post-resuscitation care has an impact on overall outcome and consists of ongoing resuscitation and organ support, neuroprotection, treatment of the cause of the cardiac arrest and management of underlying co-morbidities.
Let us deconstruct this answer. This question interrogates the candidate's ability to approach a post-arrest patient in a systematic manner. Of course, the natural tendency of any ICU trainee would be to immediately start ranting about therapeutic hypothermia (hard to blame them, of course - it is indeed an exciting topic). And then to strat ranting about family discussions. The savvy candidate will note that there is no mention of family discussions in the model answer.
The answer is organised in a familiar A-B-C-D of resuscitation. I have both a brief summary of post-resuscitation care, and a prolonged elaboration of this topic. In brief, a structured answer would resemble the following:
First, the college wants you to acknowledge that the patient is intubated, and that you are concerned about their ETT position. This, as a matter of general principle, is never wrong.
Secondly, the college wants you to acknowledge that you would pursue normoxia and normocapnea.
TTE, angiography, fluids and vasopressors are mentioned - again, this is consistent with the AHA guidelines.
Therapeutic hypothermia is mentioned, and it would be amiss to write an answer to this question without discussing this.
Overall, the model answer expects nothing suprising or inventive from the candidate. The only unusual feature is the mention of ECMO, which (unlike the rest of the answer) does not have strong evidence behind it in post-resuscitation care.
Kilgannon, J. Hope, et al. "Association between arterial hyperoxia following resuscitation from cardiac arrest and in-hospital mortality." JAMA: The Journal of the American Medical Association 303.21 (2010): 2165-2171.
Peberdy, Mary Ann, et al. "Part 9: Post–Cardiac Arrest Care 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care." Circulation 122.18 suppl 3 (2010): S768-S786.
Stub, Dion, et al. "Post Cardiac Arrest Syndrome A Review of Therapeutic Strategies." Circulation 123.13 (2011): 1428-1435.
Outline the Intensive Care management of a 25-year-old male who has fulfilled brain death criteria and is awaiting surgery for organ donation.
Temperature Maintenance:
Respiratory support:
Circulatory Support:
Immediately prior to brain death there is often a period of sympathetic hyperactivity with associated tachycardia and hypertension. This is lost following brain death commonly resulting in vasodilation and hypotension
Metabolic haematology and biochemistry:
Diabetes insipidus is common and if not recognized and treated can quickly lead to hypernatraemia and hyperosmolality
Communication:
This is a straightforward question about the care of the brain-dead organ donor. A summary exists on this site, which was derived directly from the recent ANZICS guidelines. If one were to rearrange the answer to fit some sort of primitive alphabetical template, it could resemble this:
Non-clinical issues: (presumably, these have been dealt with now that the patient is "awaiting surgery for organ donation"
Summarized from the ANZIC statement on Brain Death and Organ Donation, Version 3.2
Dujardin, Karl S., et al. "Myocardial dysfunction associated with brain death: clinical, echocardiographic, and pathologic features." The Journal of heart and lung transplantation 20.3 (2001): 350-357.
Totsuka, Eishi, et al. "Influence of high donor serum sodium levels on early postoperative graft function in human liver transplantation: effect of correction of donor hypernatremia." Liver Transplantation and Surgery 5.5 (1999): 421-428.
Novitzky, D., D. K. C. Cooper, and B. Reichart. "Hemodynamic and metabolic responses to hormonal therapy in brain-dead potential organ donors." Transplantation 43.6 (1987): 852-854.
Phongsamran, Paula. "Critical care pharmacy in donor management." Progress in Transplantation 14.2 (2004): 105-113.
RANDELL, TARJA T., and KRISTER AV HöCKERSTEDT. "TRIIODOTHYRONINE TREATMENT IN BRAIN-DEAD MULTIORGAN DONORS-A CONTROLLED STUDY." Transplantation 54.4 (1992): 736-737.
Goarin, Jean-Pierre, et al. "The effects of triiodothyronine on hemodynamic status and cardiac function in potential heart donors." Anesthesia & Analgesia 83.1 (1996): 41-47.
Follette, David M., Steven M. Rudich, and Wayne D. Babcock. "Improved oxygenation and increased lung donor recovery with high-dose steroid administration after brain death." The Journal of heart and lung transplantation: the official publication of the International Society for Heart Transplantation 17.4 (1998): 423-429.
Lisman, T., et al. "Activation of hemostasis in brain dead organ donors: an observational study." Journal of Thrombosis and Haemostasis 9.10 (2011): 1959-1965.
Lim, H. B., and M. Smith. "Systemic complications after head injury: a clinical review." Anaesthesia 62.5 (2007): 474-482.
Dalle Ave, Anne L., Dale Gardiner, and David M. Shaw. "Cardio‐pulmonary resuscitation of brain‐dead organ donors: a literature review and suggestions for practice." Transplant International (2015).
Singer, Pierre, Haim Shapiro, and Jonathan Cohen. "Brain death and organ damage: the modulating effects of nutrition." Transplantation 80.10 (2005): 1363-1368.
With regards to the determination of brain death:
a) Apart from identifying evidence of sufficient intracranial pathology, list the preconditions that must be met prior to the determination of brain death by clinical criteria:
b)What is the recommended minimum time for observation in cases of hypoxic-ischaemic brain injury, prior to performing clinical testing of brain-stem function?
c)For each of the following brainstem reflexes, list the cranial nerves that are tested:
|
a. |
Cough reflex |
|
b. |
Vestibulo-ocular reflex |
|
c. |
Pupilary light reflex |
|
d. |
Corneal reflex |
|
e. |
Gag reflex |
d) List three contraindications to performing apnoea testing:
e) List the acceptable imaging techniques that may be used to demonstrate brain death as an alternative to clinical testing as recommended by the ANZICS Statement on Death and Organ Donation.
a)
b)
24 hours
c)
|
a. |
Cough reflex |
cranial nerve X |
|
b. |
Vestibulo-ocular reflex |
cranial nerve III,IV,VI,VIII |
|
c. |
Pupilary light reflex |
cranial nerve II & III |
|
d. |
Corneal reflex |
cranial nerve V & VII |
|
e. |
Gag reflex |
cranial nerve IX & X |
(for each part of this question ALL cranial nerves are required in order to receive the 5 marks, no marks should be given for an incomplete response)
d)
e)
This question tests the candidate's detailed knowledge of the ANZICS Statement on Death and Organ Donation (I have linked to Version 3.2, from 2013).
a) Apart from identifying evidence of sufficient intracranial pathology, list the preconditions that must be met prior to the determination of brain death by clinical criteria:
The below answer is taken directly from the Statement.
b)What is the recommended minimum time for observation in cases of hypoxic-ischaemic brain injury, prior to performing clinical testing of brain-stem function?
This is an ambiguously worded question, because one could interpret is as " minimum time from cardiac arrest" or "minimum time of unresponsive coma". Quoting the ANZICS document, "There must be a minimum of four hours observation and mechanical ventilation during which the patient has unresponsive coma" before the brain-stem function can be tested. The timing of the tests following ROSC is 24 hours: "It is ... recommended that, in cases of acute hypoxic-ischaemic brain injury, clinical testing for brain death be delayed for at least 24 hours subsequent to the restoration of spontaneous circulation. "
c)For each of the following brainstem reflexes, list the cranial nerves that are tested:
|
a. |
Cough reflex |
Vagus (CN X) |
|
b. |
Vestibulo-ocular reflex |
CN III, IV, VI, and VIII |
|
c. |
Pupilary light reflex |
CN II, CN III |
|
d. |
Corneal reflex |
CN V, CN VII |
|
e. |
Gag reflex |
CN IX, CN X |
In this list the college have omitted the test for pain in the trigeminal nerve distribution (CN V and VII)
d) List three contraindications to performing apnoea testing:
The presence of any brainstem reflexes is also a contraindication. Apnoea testing must be carried out only after the brainstem reflexes have been tested, and if any of them were found to be positive any further braindeath testing cannot continue.
e) List the acceptable imaging techniques that may be used to demonstrate brain death as an alternative to clinical testing as recommended by the ANZICS Statement on Death and Organ Donation.
ANZICS Death and Organ Donation Committee, THE ANZICS STATEMENT ON DEATH AND ORGAN DONATION Edition 3.2 2013
With respect to brain death and organ dbnation as specified in the ANZICS guidelines:
a) List the pre-conditions that would preclude the determination of brain death by clinical examination. (30% marks)
b) List the components of the clinical examination to determine brain death and where appropriate the cranial nerve(s) being tested. (40% marks)
c) If clinical testing has been precluded, what investigations can be used to demonstrate a lack of intracranial blood flow? (30% marks)
a)
Conditions precluding clinical testing brain death
b)
Examination components:
Observation
Clinical test Cranial Nerve
i. Coma
ii. Pupillary reflex II, III
iii. Corneal reflex V, VII
iv. Pain reflex in trigeminal nerve distribution V, VII
v. Vestibular ocular reflex III, IV, VI, VIII
vi. Gag reflex IX, X
vii. Cough reflex X
viii. Breathing effort with apnoea
Imaging techniques
Imaging techniques need to be done in association with exclusion of preconditions and assessment of those cranial nerves that can be assessed and results need to be reviewed by 2 appropriate clinicians excluding the clinician performing the test.
a)
The below preconditions are taken directly from the ANZICS Statement.
Four hours of observation during which the patient remains in unresponsive coma
Preconditions for apnoea testing
b)
Testing for unresponsive coma
Brain Stem Reflex Testing (these are tested in sequence; all reflexes must be absent)
Apnoea testing
c)
Investigations used to demonstrate a lack of intracranial blood flow are slightly different to those which might be used to demonstrate brain death, as the lattercategory may include such things as EEG (isoelectric EEG).
The imaging modalities are discussed in greater detail in the chapter on radiological testing for brain death.
In brief, the ANZICS-recommended modalities are:
Modalities which are not recommended as strongly include:
The ANZICS statement now says CT angio "is acceptable", whereas at the time of this exam paper being written they merely weazeled that it "may be acceptable". The argument againt CT angiography is the gated timing of the scan. Whereas DSA watches contrast wash in over time in a series of still images, the CT offers a momentary snapshot of that contrast in the vessels. One might argue that the CT was mis-timed, and the contrast did not yet have time to move into the brain (in this way, perfectly healthy people could be made to appear brain-dead by adjusting the timing of the scan). Obviously, when one is going to declare brain death, there needs to be no argument about the validity of the confirmatory test. The 2014 Cochrane review (Taylor et al) could not support the use of CTA, but subsequent improvements in technology have improved the level of confidence with this modality. ANZICS now recommends the use of a four-point scale to radiologically confirm absent brain perfusion by CTA, which consists of "absent enhancement of both middle cerebral artery (MCA) cortical branches (i.e. beyond the Sylvian branches); andabsent enhancement of both internal cerebral veins"
ANZICS Statement on Death and Organ Donation
Taylor, Tim, et al. "Computed tomography (CT) angiography for confirmation of the clinical diagnosis of brain death." The Cochrane Library (2014).
You have taken over the care of a 22-year-old male admitted to ICU 3 days previously. He has sustained a severe isolated traumatic brain injury, including significant bilateral ocular injuries resulting in a ruptured globe on the right and traumatic third nerve palsy on the left.
Your colleagues report that the patient has stopped triggering the ventilator overnight and suspect that he might be brain dead.
Describe how you would diagnose brain death in this patient, including the options that are available
Ensure severity of brain injury is compatible with brain death (i.e. sufficient intracranial pathology) by reviewing relevant imaging.
Confirm that there has been a minimum of four hours observation and mechanical ventilation during which the patient has had unresponsive coma (GCS-3), no spontaneous breathing effort, absent cough/tracheal reflex.
Complete brainstem reflexes cannot be performed in this case and therefore brain death cannot be certified by clinical testing alone and will have to be determined by demonstrating absence of intracranial blood flow. However, the part of the clinical examination that can be undertaken should be performed.
Ensure that the following pre-conditions have been met in order to do limited brain death testing-
Normothermia (temperature > 35C);
Normotension (as a guide, systolic blood pressure > 90 mmHg, mean arterial pressure (MAP) > 60 mmHg in an adult);
Exclusion of effects of sedative drugs
Absence of severe electrolyte, metabolic or endocrine disturbances
Intact neuromuscular function
Ability to perform apnoea testing
Undertake the clinical tests that can be done
Response to painful stimulus to four limbs and trunk.
Response to pain in trigeminal nerve distribution
Gag reflex
Cough reflex
Apnoea testing
* Pupillary, corneal and cold caloric reflexes cannot be tested.
If all above reflexes absent, proceed to 4-vessel intra-arterial catheter angiography. Blood flow should not be demonstrable above the level of the carotid siphon in the anterior circulation, or above the foramen magnum in the posterior circulation
Alternatives-
Radionuclide imaging with Technetium -99m radiolabelled hexamethyl propylene amine oxime. (Tc-99mHMPAO)
Contrast CT or CT-angiography subject to specific radiologic diagnostic guidelines. (Absent enhancement bilaterally of all of the following are likely to be the most reliable early CT indicators of brain death: middle cerebral artery cortical branches — that is beyond the Sylvian branches; P2 segment of the posterior cerebral arteries; pericallosal arteries; and internal cerebral veins)
Brain death can then be certified by 2 medical practitioners (not including the practitioner who performed the imaging investigation) who have examined the patient and have knowledge of the circumstances of the coma
Important points in the answer:
Confirmation of a diagnosis compatible with brain death
Why clinical testing will not be sufficient
Preconditions satisfied
List of clinical tests that can be performed
Details of imaging test of choice + list of 2 alternatives
Detailed radiologic features required for diagnosis on contrast CT was not required, but an indication that specific radiologic criteria exist was expected.
Confirmation with clinical testing alone was considered a fatal error.
The diagnosis of brain death should be the bread and butter of an ICU specialist (as it is the thing that we do which is sufficiently unique to be the domain of intensivists alone). It is therefore surprising that only 43% of the candidates scored a passing mark. The college answer is remarkable in that it offers us a glimpse of the normally hidden marking rubric for an SAQ.
To break down this rubric into answerable components:
Confirmation of a diagnosis compatible with brain death
Why clinical testing will not be sufficient
Preconditions satisfied
List of clinical tests that can be performed
One needs to be reminded that the ANZICS statement recommends clinical testing should still be attempted: "If a complete examination is not possible (e.g. eye or ear trauma) or apnoea testing precluded (e.g. severe lung injury or high cervical trauma), then that part of the clinical examination that can be performed, should be undertaken".
Details of imaging test of choice + list of 2 alternatives
You are performing clinical brain death testing on a 63-year-old male. Two arterial blood gas (ABG) results are presented below. ABG 1 was performed immediately prior to testing, and ABG 2 was performed at the end of the apnoea test.
a) Comment on the implication these results have for diagnosing brain death in this patient. (20% marks)
|
Parameter |
Patient Value |
Adult Normal Range |
|
|
ABG 1 |
ABG 2 |
||
|
FiO2 |
0.4 |
1.0 |
|
|
pH |
7.41 |
7.32* |
7.35 – 7.45 |
|
pO2 |
110 mmHg (14.7 kPa) |
148 mmHg (19.7 kPa) |
|
|
pCO2 |
49.0 mmHg (6.5 kPa)* |
62.0 mmHg (8.3 kPa)* |
35.0 – 45.0 (4.6 – 6.0) |
|
SpO2 |
96% |
97% |
|
|
Bicarbonate |
30.0 mmol/L* |
31.0 mmol/L* |
22.0 – 26.0 |
|
Base Excess |
5.3 mmol/L* |
4.9 mmol/L* |
-2.0 – +2.0 |
|
Lactate |
1.8 mmol/L* |
1.8 mmol/L* |
0.5 – 1.6 |
|
Sodium |
151 mmol/L* |
152 mmol/L* |
135 – 145 |
|
Potassium |
4.2 mmol/L |
4.1 mmol/L |
3.5 – 5.0 |
|
Chloride |
103 mmol/L |
102 mmol/L |
95 – 105 |
|
Glucose |
7.5 mmol/L* |
8.1 mmol/L* |
3.5 – 6.0 |
a)
Although the CO2 has risen to above 60 mmHg, the pH remains above 7.3, and so brain death cannot be diagnosed. The Na of 152 does not preclude the diagnosis of brain death.
This question is straight from the CICM ANZICS statement (version 3.2) which reads:
"At the end of the period without mechanical ventilation, apnoea must persist in the presence of an adequate stimulus to spontaneous ventilation, i.e. an arterial PaCO2 > 60 mmHg (8 kPa) and an arterial pH < 7.30"
The key point there is an arterial PaCO2 > 60 mmHg (8 kPa) and an arterial pH < 7.30. Both must be demonstrated in order for the clinical diagnosis of brain death to be valid. As to why and how this was decided, the ANZICS statement is silent. The American guidelines do not contain this rule.
Interestingly, as a reader had pointed out, there is more material in this blood gas result to discredit the apnoea test result. Consider the pre-test bicarbonate value, which is 31 mmol/L. The PaCO2 is only 49 at this stage, but surely the high baseline bicarbonate means there must be some sort of chronic CO2 retention here. And if so, you'd want the PaCO2 to rise by at least 20 mmHg (i.e. up to 69 mmHg) in order to be able to declare the apnoea test as failed, considering that the ANZICS statement clearly says:
"In patients with pre-existing hypercapnia, it is recommended to wait for a PaCO₂ rise of >20 mmHg (2.7 Kpa) above the chronic level, with a pH <7.30."
This did not happen in the example, and the high initial bicarbonate may also to some extent account for the pH being higher than 7.30 at the end of the test.
As for the sodium level, the old ANZICS statement was not prescriptive; "marked derangements" were disqualifying, but there no was mention as to how marked these must be. The new Version 4 of the statement gives the following ranges:
Other Intensive Care Societies differ slightly; for example the Irish ICSI guidelines recommend 125-155mmol/L as the acceptable range for clinical testing.
ANZICS Death and Organ Donation Committee, THE ANZICS STATEMENT ON DEATH AND ORGAN DONATION Edition 3.2 2013
Wijdicks, Eelco FM, et al. "Evidence-based guideline update: determining brain death in adults: report of the Quality Standards Subcommittee of the American Academy of Neurology." Neurology 74.23 (2010): 1911-1918.
Thanks to Simon Baylis for picking up the chronic hypercapnia which was hidden in plain sight here.
Outline the ICU management of a 25-year-old male who has fulfilled brain death criteria and is awaiting surgery for organ donation.
Not available.
Summarized from the ANZIC statement on Brain Death and Organ Donation, Version 3.2
Dujardin, Karl S., et al. "Myocardial dysfunction associated with brain death: clinical, echocardiographic, and pathologic features." The Journal of heart and lung transplantation 20.3 (2001): 350-357.
Totsuka, Eishi, et al. "Influence of high donor serum sodium levels on early postoperative graft function in human liver transplantation: effect of correction of donor hypernatremia." Liver Transplantation and Surgery 5.5 (1999): 421-428.
Novitzky, D., D. K. C. Cooper, and B. Reichart. "Hemodynamic and metabolic responses to hormonal therapy in brain-dead potential organ donors." Transplantation 43.6 (1987): 852-854.
Phongsamran, Paula. "Critical care pharmacy in donor management." Progress in Transplantation 14.2 (2004): 105-113.
RANDELL, TARJA T., and KRISTER AV HöCKERSTEDT. "TRIIODOTHYRONINE TREATMENT IN BRAIN-DEAD MULTIORGAN DONORS-A CONTROLLED STUDY." Transplantation 54.4 (1992): 736-737.
Goarin, Jean-Pierre, et al. "The effects of triiodothyronine on hemodynamic status and cardiac function in potential heart donors." Anesthesia & Analgesia 83.1 (1996): 41-47.
Follette, David M., Steven M. Rudich, and Wayne D. Babcock. "Improved oxygenation and increased lung donor recovery with high-dose steroid administration after brain death." The Journal of heart and lung transplantation: the official publication of the International Society for Heart Transplantation 17.4 (1998): 423-429.
Lisman, T., et al. "Activation of hemostasis in brain dead organ donors: an observational study." Journal of Thrombosis and Haemostasis 9.10 (2011): 1959-1965.
Lim, H. B., and M. Smith. "Systemic complications after head injury: a clinical review." Anaesthesia 62.5 (2007): 474-482.
Dalle Ave, Anne L., Dale Gardiner, and David M. Shaw. "Cardio‐pulmonary resuscitation of brain‐dead organ donors: a literature review and suggestions for practice." Transplant International (2015).
Singer, Pierre, Haim Shapiro, and Jonathan Cohen. "Brain death and organ damage: the modulating effects of nutrition." Transplantation 80.10 (2005): 1363-1368.
List the clinical signs and tests used for neuro-prognostication after cardiac arrest and discuss their limitations.
Not available.
The question did not ask for "advantages and disadvantages", they only wanted limitations. Thus, a mangled truncated version of summary the table from the neuroprognostication chapter is offered here.
| Predictive sign or investigation | Limitations and confounding factors |
| Absent pupillary reflex |
|
| Absent corneal reflex | |
| Extensor motor response, or worse |
|
| Myoclonic status epilepticus |
|
| Somatosensory evoked potentials: absence of the N20 component |
|
| Burst suppression on EEG |
|
| Absence of EEG reactivity, or "malignant" EEG pattern |
|
| Neuron-specific enolase |
|
| CT brain |
|
| MRI brain |
|
Engdahl, Johan, et al. "Can we define patients with no and those with some chance of survival when found in asystole out of hospital?." The American journal of cardiology 86.6 (2000): 610-614.
Bunch, T. Jared, et al. "Outcomes and in-hospital treatment of out-of-hospital cardiac arrest patients resuscitated from ventricular fibrillation by early defibrillation." Mayo Clinic Proceedings. Vol. 79. No. 5. Elsevier, 2004.
Levine, Robert L., Marvin A. Wayne, and Charles C. Miller. "End-tidal carbon dioxide and outcome of out-of-hospital cardiac arrest." New England Journal of Medicine 337.5 (1997): 301-306.
Rea, Thomas D., et al. "Temporal Trends in Sudden Cardiac Arrest A 25-Year Emergency Medical Services Perspective." Circulation 107.22 (2003): 2780-2785.
Carew, Heather T., Weiya Zhang, and Thomas D. Rea. "Chronic health conditions and survival after out-of-hospital ventricular fibrillation cardiac arrest." Heart 93.6 (2007): 728-731.
Goldberger, Zachary D., et al. "Duration of resuscitation efforts and survival after in-hospital cardiac arrest: an observational study." The Lancet (2012).
Wijdicks, E. F. M., et al. "Practice Parameter: Prediction of outcome in comatose survivors after cardiopulmonary resuscitation (an evidence-based review) Report of the Quality Standards Subcommittee of the American Academy of Neurology."Neurology 67.2 (2006): 203-210.
Rogove, Herbert J., et al. "Old age does not negate good cerebral outcome after cardiopulmonary resuscitation: analyses from the brain resuscitation clinical trials."Critical care medicine 23.1 (1995): 18-25.
LEVY, DE, et al. "Predicting Outcome from Hypoxic-Ischemic Coma." Survey of Anesthesiology 30.2 (1986): 93.
Sandroni, Claudio, et al. "Prognostication in comatose survivors of cardiac arrest: an advisory statement from the European Resuscitation Council and the European Society of Intensive Care Medicine." Resuscitation 85.12 (2014): 1779-1789.
Greer, David M., et al. "Clinical examination for prognostication in comatose cardiac arrest patients." Resuscitation 84.11 (2013): 1546-1551.
Lee, Ha Lim, and Ju Kang Lee. "Lance-adams syndrome." Annals of rehabilitation medicine 35.6 (2011): 939-943.
Bouwes, Aline, et al. "Acute posthypoxic myoclonus after cardiopulmonary resuscitation." BMC neurology 12.1 (2012): 63.
Stammet, Pascal, et al. "Neuron-specific enolase as a predictor of death or poor neurological outcome after out-of-hospital cardiac arrest and targeted temperature management at 33 C and 36 C." Journal of the American College of Cardiology 65.19 (2015): 2104-2114.
Golan, Eyal, et al. "Predicting Neurologic Outcome After Targeted Temperature Management for Cardiac Arrest: Systematic Review and Meta-Analysis*." Critical care medicine 42.8 (2014): 1919-1930.
Howes, Daniel, et al. "Canadian Guidelines for the use of targeted temperature management (therapeutic hypothermia) after cardiac arrest: A joint statement from The Canadian Critical Care Society (CCCS), Canadian Neurocritical Care Society (CNCCS), and the Canadian Critical Care Trials Group (CCCTG)." Resuscitation 98 (2016): 48-63.
Sandroni, Claudio, Sonia D’Arrigo, and Jerry P. Nolan. "Prognostication after cardiac arrest." Critical care 22.1 (2018): 1-9.
Nolan, Jerry P., et al. "European resuscitation council and european society of intensive care medicine guidelines 2021: post-resuscitation care." Resuscitation 161 (2021): 220-269.
Cronberg, Tobias, et al. "Brain injury after cardiac arrest: from prognostication of comatose patients to rehabilitation." The Lancet Neurology 19.7 (2020): 611-622.
Kim, Youn-Jung, et al. "Long-term neurological outcomes in patients after out-of-hospital cardiac arrest." Resuscitation 101 (2016): 1-5.
Scarpino, Maenia, et al. "Neurophysiology and neuroimaging accurately predict poor neurological outcome within 24 hours after cardiac arrest: the ProNeCA prospective multicentre prognostication study." Resuscitation 143 (2019): 115-123.
Dyson, Kylie, et al. "International variation in survival after out-of-hospital cardiac arrest: a validation study of the Utstein template." Resuscitation 138 (2019): 168-181.
Dragancea, Irina, et al. "The influence of induced hypothermia and delayed prognostication on the mode of death after cardiac arrest." Resuscitation 84.3 (2013): 337-342.
Hofmeijer, Jeannette, et al. "Unstandardized treatment of electroencephalographic status epilepticus does not improve outcome of comatose patients after cardiac arrest." Frontiers in neurology 5 (2014): 39.
Critically evaluate the role of therapeutic hypothermia following out of hospital cardiac arrest.
Not available.
Rationale:
Advantages:
Disadvantages:
Evidence:
Society recommendations
Own practice:
Bernard, Stephen A., et al. "Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia." New England Journal of Medicine346.8 (2002): 557-563. The famous study from Melbourne.
"Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest." N Engl J Med
2002; 346: 549–56
Bernard, Stephen A., and Michael Buist. "Induced hypothermia in critical care medicine: a review." Critical care medicine 31.7 (2003): 2041-2051.
Nielsen, Niklas, et al. "Targeted temperature management at 33 C versus 36 C after cardiac arrest." New England Journal of Medicine 369.23 (2013): 2197-2206.
Hypothermia after Cardiac Arrest Study Group. "Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest." New England Journal of Medicine 346.8 (2002): 549-556.
Lascarrou, J. B., et al. "Targeted Temperature Management for Cardiac Arrest with Nonshockable Rhythm" N Engl J Med 381.24 (2019): 2327-2337.
Dankiewicz, Josef, et al. "Hypothermia versus Normothermia after Out-of-Hospital Cardiac Arrest." New England Journal of Medicine 384.24 (2021): 2283-2294.
An ICU patient is suitable for consideration of donation after circulatory determination of death (DCDD).
a) Outline the process of determination of death in these patients. (30% marks)
b) Define the term ‘functional warm ischaemic time’ and discuss its significance to subsequent graft function. (40% marks)
c) Compare and contrast graft survival rates in recipients of kidney, liver, heart, and lung transplantation from DCDD and from donation after neurological determination of death. (30% marks)
This area of clinical practice is learned in mandatory CICM curriculum workshops, and therefore understanding of the process for determination of death in DCD patients should be well understood. The definition of functional warm ischemia time was incorrectly defined by most candidates, and knowledge of graft survival between different organs was also commonly incorrect.
The exam candidate, task-focused and stressed, will probably ignore the fact that this question would have worked just as well without the one-line clinical scenario posed in the stem. "An ICU patient is suitable for consideration of donation after circulatory determination of death (DCDD)" even omits "organ" from "donation", which is even more curious. Were we expected to hang our answer off this slender twig? Hard to say. What follows has not made any attempt to address any clinical scenario. Fortunately everything needed to answer this question is easily available from the ANZICS statement.
a) The process of determination of death:
The determination of death requires the patient to be:
After this point, death should be documented using a specific form.
b) Functional warm ischaemic time:
"The functional warm ischaemic time is the time from when the systolic blood pressure falls below 50 mmHg after withdrawal of cardiorespiratory support to cold perfusion and may be a better measure of ischaemic injury" (according to the latest ANZICS statement)
The effect of this time is to delay the recovery of graft function, or make donation impossible if the specific time for each organ is exceeded:
c) Graft survival: DCDD vs DNDD:
ANZICS statement - the current version at the time of writing was 4.1 but you can always get the latest one from this ANZICS page
a) List the preconditions for performing neurological determination of death by clinical brain death testing. (6 marks)
b) List the criteria for the circulatory determination of death in the context of organ donation. (4 marks)
Syllabus topic/section:
2.1.15 Organ and tissue Donation in Intensive Care: / Neurological determination of death: L1
2.2.15 Organ and tissue Donation in Intensive Care / Circulatory determination of death: L1
Discussion: Part A was in general well answered and several candidates demonstrated a very high standard by taking a structured approach following the well-known and existing guidelines. A caution to candidates to be very specific in your answer e.g. detailing the value of electrolytes and temperature including a rationale with potential challenges rather than simply stating “normal electrolytes and normothermia”. Organ and tissue donation is a key core discipline area in Intensive Care and thorough explicit detail is required to demonstrate safe clinical practice.
Unfortunately, part B was poorly answered with the inability to describe the criteria for DCD highlighting a lack of familiarity with clinical experience and senior decision making. We recommend improving your answer by following the structure of the ANZICS guidelines. This topic is very clearly documented, and the answer template is a close ally of the source document.d.
This item of core knowledge is concretely codified in fundamental CICM lore as the ANZICS statement on death and organ donation, a definitive document that does not permit any variation in practice. It is therefore not surprising that all trainees were expected to be able to answer it well, as suggested by the high Angoff cutoff. The SAQ is in fact absolutely presdcriptive, as its wording references specific sections of the Statement:
And as the Statement itself is extremely carefully worded to avoid ambiguity, this means that any creative variation in wording, where it deviates from the Statement, would have been wasteful at best, and inaccurate at worst. To regurgitate the Statement verbatim would have therefore been the best strategy; which is another way of saying "this topic is very clearly documented, and the answer template is a close ally of the source document".
a) Preconditions for performing neurological determination of death clinically:
b) Criteria for the circulatory determination of death
ANZICS statement on death and organ donation is the only reference required to complete this SAQ:
Section 1.2.1 is where your find the criteria for neurological determination
Section 1.31 is where your find the criteria for circulatory determination